Slow inward current and cardiac arrhythmias

Robert F. Gilmour, Douglas P. Zipes

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

The slow inward current contributes to the normal electrical and contractile activity of several cardiac and vascular tissues and also may mediate the electrical abnormalities responsible for certain cardiac arrhythmias. The slow inward current differs from the fast inward sodium current in that it is carried primarily by calcium rather than sodium, requires a more positive level of membrane potential to be activated, has slower activation and inactivation kinetics, is responsible for normal depolarization in sinus and atrjoventricular (AV) nodal cells and is blocked by a rather specific group of agents that includes verapamil, diltiazem and nifedipine. Recent data suggest that slow-channel openings occur in bursts, separated by silent periods, and that less negative membrane potentials and beta-adrenergic stimulation increase the probability that the channels will open. Inactivation of the channels is associated with a lower probability of channel opening. Slow-channel blocking agents such as verapamil, diltiazem and nifedipine appear to bind to activated, rather than rested, slow channels. Therefore, their effects are more prominent at faster pacing rates and at less negative membrane potentials. Clinically occurring cardiac arrhythmias dependent on the slow inward current include primarily sinus and AV nodal reentry and reciprocating tachycardia in the Wolff-Parkinson-White syndrome when one of the pathways incorporates the AV node. Damaged atrial, ventricular and specialized tissue also can generate slow response-mediated reentry or forms of automaticity that may be clinically important under certain circumstances.

Original languageEnglish
JournalThe American Journal of Cardiology
Volume55
Issue number3
DOIs
StatePublished - Jan 25 1985

Fingerprint

Membrane Potentials
Cardiac Arrhythmias
Diltiazem
Nifedipine
Verapamil
Sodium
Reciprocating Tachycardia
Wolff-Parkinson-White Syndrome
Adrenergic Agents
Blood Vessels
Calcium

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Slow inward current and cardiac arrhythmias. / Gilmour, Robert F.; Zipes, Douglas P.

In: The American Journal of Cardiology, Vol. 55, No. 3, 25.01.1985.

Research output: Contribution to journalArticle

Gilmour, Robert F. ; Zipes, Douglas P. / Slow inward current and cardiac arrhythmias. In: The American Journal of Cardiology. 1985 ; Vol. 55, No. 3.
@article{87e269fddd88487da4d140d1e158cd29,
title = "Slow inward current and cardiac arrhythmias",
abstract = "The slow inward current contributes to the normal electrical and contractile activity of several cardiac and vascular tissues and also may mediate the electrical abnormalities responsible for certain cardiac arrhythmias. The slow inward current differs from the fast inward sodium current in that it is carried primarily by calcium rather than sodium, requires a more positive level of membrane potential to be activated, has slower activation and inactivation kinetics, is responsible for normal depolarization in sinus and atrjoventricular (AV) nodal cells and is blocked by a rather specific group of agents that includes verapamil, diltiazem and nifedipine. Recent data suggest that slow-channel openings occur in bursts, separated by silent periods, and that less negative membrane potentials and beta-adrenergic stimulation increase the probability that the channels will open. Inactivation of the channels is associated with a lower probability of channel opening. Slow-channel blocking agents such as verapamil, diltiazem and nifedipine appear to bind to activated, rather than rested, slow channels. Therefore, their effects are more prominent at faster pacing rates and at less negative membrane potentials. Clinically occurring cardiac arrhythmias dependent on the slow inward current include primarily sinus and AV nodal reentry and reciprocating tachycardia in the Wolff-Parkinson-White syndrome when one of the pathways incorporates the AV node. Damaged atrial, ventricular and specialized tissue also can generate slow response-mediated reentry or forms of automaticity that may be clinically important under certain circumstances.",
author = "Gilmour, {Robert F.} and Zipes, {Douglas P.}",
year = "1985",
month = "1",
day = "25",
doi = "10.1016/0002-9149(85)90617-4",
language = "English",
volume = "55",
journal = "American Journal of Cardiology",
issn = "0002-9149",
publisher = "Elsevier Inc.",
number = "3",

}

TY - JOUR

T1 - Slow inward current and cardiac arrhythmias

AU - Gilmour, Robert F.

AU - Zipes, Douglas P.

PY - 1985/1/25

Y1 - 1985/1/25

N2 - The slow inward current contributes to the normal electrical and contractile activity of several cardiac and vascular tissues and also may mediate the electrical abnormalities responsible for certain cardiac arrhythmias. The slow inward current differs from the fast inward sodium current in that it is carried primarily by calcium rather than sodium, requires a more positive level of membrane potential to be activated, has slower activation and inactivation kinetics, is responsible for normal depolarization in sinus and atrjoventricular (AV) nodal cells and is blocked by a rather specific group of agents that includes verapamil, diltiazem and nifedipine. Recent data suggest that slow-channel openings occur in bursts, separated by silent periods, and that less negative membrane potentials and beta-adrenergic stimulation increase the probability that the channels will open. Inactivation of the channels is associated with a lower probability of channel opening. Slow-channel blocking agents such as verapamil, diltiazem and nifedipine appear to bind to activated, rather than rested, slow channels. Therefore, their effects are more prominent at faster pacing rates and at less negative membrane potentials. Clinically occurring cardiac arrhythmias dependent on the slow inward current include primarily sinus and AV nodal reentry and reciprocating tachycardia in the Wolff-Parkinson-White syndrome when one of the pathways incorporates the AV node. Damaged atrial, ventricular and specialized tissue also can generate slow response-mediated reentry or forms of automaticity that may be clinically important under certain circumstances.

AB - The slow inward current contributes to the normal electrical and contractile activity of several cardiac and vascular tissues and also may mediate the electrical abnormalities responsible for certain cardiac arrhythmias. The slow inward current differs from the fast inward sodium current in that it is carried primarily by calcium rather than sodium, requires a more positive level of membrane potential to be activated, has slower activation and inactivation kinetics, is responsible for normal depolarization in sinus and atrjoventricular (AV) nodal cells and is blocked by a rather specific group of agents that includes verapamil, diltiazem and nifedipine. Recent data suggest that slow-channel openings occur in bursts, separated by silent periods, and that less negative membrane potentials and beta-adrenergic stimulation increase the probability that the channels will open. Inactivation of the channels is associated with a lower probability of channel opening. Slow-channel blocking agents such as verapamil, diltiazem and nifedipine appear to bind to activated, rather than rested, slow channels. Therefore, their effects are more prominent at faster pacing rates and at less negative membrane potentials. Clinically occurring cardiac arrhythmias dependent on the slow inward current include primarily sinus and AV nodal reentry and reciprocating tachycardia in the Wolff-Parkinson-White syndrome when one of the pathways incorporates the AV node. Damaged atrial, ventricular and specialized tissue also can generate slow response-mediated reentry or forms of automaticity that may be clinically important under certain circumstances.

UR - http://www.scopus.com/inward/record.url?scp=0021992484&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0021992484&partnerID=8YFLogxK

U2 - 10.1016/0002-9149(85)90617-4

DO - 10.1016/0002-9149(85)90617-4

M3 - Article

VL - 55

JO - American Journal of Cardiology

JF - American Journal of Cardiology

SN - 0002-9149

IS - 3

ER -